Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 420, Issue 2, Pages 293-296Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2012.02.152
Keywords
Cdc25A; NF-kappa B; I kappa-B alpha; Ubiquitination; Apoptosis
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Funding
- National Research Foundation of Korea(NRF)
- Ministry of Education, Science and Technology [2009-0072203]
- National Research Foundation of Korea [2009-0072203] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Cell division cycle 25A (Cdc25A), a dual specificity protein phosphatase, exhibits anti-apoptotic activity, but the underlying molecular mechanisms are poorly characterized. Here we report that Cdc25A inhibits cisplatin-induced apoptotic cell death by stimulating nuclear factor-kappa B (NF-kappa B) activity. In HEK-293 cells, Cdc25A decreased protein level of inhibitor subunit kappa B alpha (I kappa-B alpha) in association with increased serine 32-phosphorylation, followed by stimulation of transcriptional activity of NF-kappa B. Inhibition of NF-kappa B activity by chemical inhibitor or overexpression of I kappa-B alpha in Cdc25A-elevated cancer cells resistant to cisplatin improved their sensitivity to cisplatin-induced apoptosis. Our data show for the first time that Cdc25A has an important physiological role in NF-kappa B activity regulation and it may be an important survival mechanism of cancer cells. (C) 2012 Elsevier Inc. All rights reserved.
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